Serum creatine kinase activity following forearm flexion isometric exercise

The purpose of this study was to compare serum creatine kinase (CK) activity following two forearm flexion isometric exercise regimens differing in work to rest ratio, and examine the CK response to a repeated bout of isometric exercise. Eleven males were tested on two sessions (bouts) spaced 1 week apart. For bout 1, five subjects (group A) performed a forearm flexion isometric exercise consisting of 40 10-s maximal contractions with 20-s inter-trial rests (10:20), while six (group B) performed 40 maximal 10-s contractions with 5-s inter-trial rests (10:5). The increase in serum CK activity following the 10:20 exercise (143%) was significantly greater than that following the 10:5 exercise (52%). The 10:20 exercise was also associated with greater tension generation over trials. One week later, both groups performed a bout of 10:20 exercise. A substantial reduction in the serum CK response was found following this second bout. The data suggest that for bout 1 the isometric exercise associated with the greater overall tension levels resulted in the greater CK response. However, when the 10:20 exercise was repeated 1 week later, a substantial reduction in the CK response was found which was unrelated to the tension generated.     

Effect of resistance exercise on dehydroepiandrosterone sulfate concentrations during a 72-h recovery: relation to glucose tolerance and insulin response

Serum dehydroepiandrosterone sulfate (DHEA-S) concentration is known to be associated with the whole-body insulin sensitivity. The main purpose of the study was to investigate the effect of resistance exercise on DHEA-S concentration during a 72 h post-exercise recovery, and its relation to glucose tolerance and insulin sensitivity. Morning fasted serum samples was obtained from 19 male volunteers (aged 21.1+/-0.4 years) 24 h before the onset of exercise and 24 h, 48 h, and 72 h following exercise for measurements of DHEA-S, cortisol, and TNF-alpha. Oral glucose tolerance test (OGTT) and insulin response were determined 24 h before and 48 h after exercise. We found that resistance exercise causes a delayed suppression in serum DHEA-S levels during recovery (48 h and 72 h). This exercise challenge did not affect glucose tolerance, but insulin response during OGTT was significantly elevated. The increased insulin level was not associated with serum levels of cortisol and TNF-alpha. In conclusion, the present study found that resistance exercise has a DHEA-S lowering effect that persisted for 72 h. This change could be related to the elevated insulin concentrations during OGTT.     

Effect of a single bout of acute exercise on plasma human immunodeficiency virus RNA levels.

Acute exercise is known to activate the immune system and thus could lead to increased human immunodeficiency virus (HIV) replication. We sought to determine whether a single acute bout of exercise, similar to what people experience when starting an intensive exercise program, has a detrimental effect on plasma HIV RNA levels. Twenty-five patients with HIV infection performed one 15-min bout of acute exercise. Absolute neutrophil counts, serum creatine phosphokinase, and 72-h urinary 3-methylhistidine (a marker of muscle protein breakdown) were measured before and after the exercise, along with plasma HIV RNA levels. There were increases in neutrophil counts (P < 0.06), serum creatine phosphokinase (P < 0. 01), and urinary 3-methylhistidine (P < 0.01) in response to exercise, indicating a mild acute-phase response with muscle proteolysis. However, mean HIV RNA, which was elevated at baseline in 22 of the 25 subjects (mean of 4 x 10(5) +/- 0.7 x 10(5) copies/ml), did not increase during the week after exercise (P = 0. 12). Small changes in RNA were seen in the three subjects with initially undetectable HIV RNA, but the significance of these changes is unclear. Acute exercise does not have a deleterious effect on HIV replication in adults with high viral loads. Because regular exercise training has not been shown to activate the acute-phase response, the lack of increased viral loads in response to an acute exercise intervention suggests that exercise training is safe in people with HIV infection.     

Effect of exercise-induced hyperthermia on serum iron concentration

Serum iron levels have been shown to decline both with fever and with strenuous exercise, leading to the supposition that the decrease might be the result of a rise in core body temperature. To evaluate this hypothesis, the serum iron response to an exercise-induced 1.5°C rise in core body temperature was measured. To increase core temperature, five females and two males exercised in an environmental chamber heated to 41°C with a relative humidity of 40%. Blood samples were taken before exercise and immediately after body temperature increased approximately 1.5°C. Blood was also collected 1 h, 6 h, and 24 h postexercise. Results showed that the core body temperature significantly increased (p<0.001) from a mean baseline value of 36.5±0.1°C to 38.1±0.1°C following exercise. A one-way repeated measures analysis of variance was used to examine the effect of increased core body temperature on serum iron levels over the five time periods: preexercise, immediate postexercise, and 1 h, 6 h, and 24 h postexercise. The results indicated that there were no significant differences in serum iron levels among time periods. This suggests that the previously reported depression of serum iron levels that occurs with fever and after prolonged exercise is not the result of hyperthermia. Rather, the change in serum iron occurs in response to biological or physiological stressors, such as bacterial infection, muscle damage, or unusual trauma. Further studies are needed to explicate the mechanisms responsible for these changes.     

Effect of incremental exercise on airway and systemic inflammation in patients with COPD

Airway and systemic inflammation are features of chronic obstructive pulmonary disease (COPD), and there is growing interest in clarifying the inflammatory processes. Strenuous exercise induces an intensified systemic inflammatory response in patients with COPD, but no study has investigated the airway inflammatory and anti-inflammatory responses to exercise. Twenty steroid-na?ve, ex-smokers with diagnosed COPD (forced expired volume in 1 s = 66 ± 12%) underwent baseline collection of venous blood and induced sputum followed by an incremental exercise test to symptom limitation 48 h later. Additional venous blood samples were collected following exercise at 0, 2, and 24 h, while induced sputum was collected 2 and 24 h after exercise. Sputum and blood samples were analyzed for differential cell count, CD4(+) and CD8(+) T lymphocytes (serum only), interleukin (IL)-6, IL-8, IL-10, chemokine (C-C motif) ligand 5 (CCL5), and high sensitivity C-reactive protein (serum only). There was an increase in the number of sputum eosinophils (cells/gram, P = 0.012) and a reduction in sputum IL-6 (P = 0.01) 24 h postexercise. Sputum IL-8 and CCL5 were also persistently decreased after exercise (P = 0.0098 and P = 0.0012, respectively), but sputum IL-10 did not change. There was a decrease in serum eosinophils 2 h after exercise (P = 0.0014) and a reduction in serum CCL5 immediately following and 2 h postexercise (P < 0.0001). Both serum eosinophils and CCL5 returned to baseline levels within 24 h. An acute bout of exercise resulted in a significant increase in the number of sputum eosinophils, which may be mediated by serum CCL5. However, there was also a reduction in sputum proinflammatory cytokines, suggesting some anti-inflammatory effect of exercise in the lungs of steroid-na?ve patients with COPD.     

Effects of exercise on immune functions of undernourished mice.

Regular moderate exercise may modulate the response to a stressor and thus improve immune functions in conditions commonly associated with immunodepression and elevated levels of stress hormones. For example, anorexia nervosa patients, many of whom engage in regular aerobic exercise, generally have normal immune function and viral disease resistance in spite of their severe undernutrition. To test the hypothesis that exercise can prevent undernutrition-induced immunodepression, mice were fed a nutritionally complete, semi-purified diet, either ad libitum or in restricted quantities to induce 25% loss of initial weight over 3 weeks. Half the animals from each dietary group were run on a treadmill for 30 min/day, 5 days/week. Exercise had no effect on several measures of nutritional status. Spleen weight and blastogenic response to lipopolysaccharide were significantly increased by exercise in undernourished mice. In vivo antibody response to sheep red blood cells, and in vitro splenic responses to concanavalin A and phytohemagglutin were not significantly affected by exercise. Serum corticosterone level was increased by food restriction and significantly decreased by exercise in the undernourished mice. Within a treatment group there were no significant correlations between serum corticosterone level and any immune system measure. Hypothalamic concentration of uric acid was increased in food restriction groups and concentration of norepinephrine was increased in exercise groups. The results suggest that regular exercise may help prevent undernutrition-induced immunodepression, possibly through modulation of the stress response.     

Beta-endorphin/beta-lipotropin release and gonadotropin secretion after acute exercise in physically conditioned males

beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) concentrations were measured in the basal state and after acute exercise for 15 min or until exhaustion in 6 physically conditioned male volunteers. Serum concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone and prolactin were also measured in the basal state. In addition, the concentrations of the gonadotropins (LH and FSH) were determined after exercise and the gonadotropin response to gonadotropin releasing hormone was assessed before and after exercise. The data show that acute exercise stimulates the release of both beta-EP and beta-LPH which return to base-line levels within 60 min after exercise. This is in contrast to our previously described results in physically unconditioned male volunteers in whom only beta-LPH release was noted after exercise. Serum LH concentrations declined after exercise reaching nadir values between 60 to 150 min after exercise. As we previously reported in physically unconditioned male volunteers, serum FSH concentrations did not change with exercise and the gonadotropin response to LRH stimulation was uninfluenced by exercise. Serum testosterone and prolactin concentration were within the normal range for healthy adult males. We speculate that the difference in beta-EP release with exercise in physically conditioned and unconditioned males represents a difference in processing of the opioid precursor molecule (pro-opiomelanocortin, POMC) in the two groups.     

Antioxidant supplementation influences the neutrophil tocopherol associated protein expression, but not the inflammatory response to exercise

Intense exercise induces inflammatory-like changes and oxidative stress in immune cells. Our aim was to study the effects of antioxidant diet supplementation on the neutrophil inflammatory response and on the tocopherol associated protein (TAP) expression after exhaustive exercise. Fourteen male-trained amateur runners were randomly divided in two placebo and supplemented groups. Vitamins C (152 mg/d) and E (50 mg/d) supplementation were administrated to the athletes for a month, using an almond based isotonic and energetic beverage. Non-enriched beverage was given to the placebo group. After one month, the subjects participated in a half-marathon race (21 km-run). Neutrophil TAP mRNA expression and markers of the inflammatory response were determined before, immediately after, and 3 h after finishing the half-marathon race. TAP expression increased after exercise mainly in the neutrophils of the placebo group. Exercise induced an inflammatory response in both placebo and supplemented groups, manifested with neutrophilia, increased creatine kinase and lactate dehydrogenase serum activities, neutrophil luminol chemiluminescence and myeloperoxidase release. Plasma malondialdehyde only increased in the placebo group after exercise. Diet supplementation with moderate levels of antioxidant vitamins avoids plasma damage in response to exhaustive exercise without the effects on the inflammatory process. Neutrophil degranulation and increased tocopherol associated protein could contribute to the neutrophil protection from the oxidative stress.     

Reduced exercise-associated response of the GH-IGF-I axis and catecholamines in obese children and adolescents.

Obesity blunts catecholamine and growth hormone (GH) responses to exercise in adults, but the effect of obesity on these exercise-associated hormonal responses in children is unclear. Therefore, the aim of the present study was to asses the effect of childhood obesity on the counterregulatory hormonal response to acute exercise. Twenty-five obese children (Ob; body mass index > 95%), and 25 age, gender, and maturity-matched normal-weight controls (NW) participated in the study. Exercise consisted of ten 2-min bouts of constant-cycle ergometry above the anaerobic threshold, with 1-min rest intervals between each bout. Pre-, post-, and 120-min postexercise blood samples were collected for circulating components of the GH-IGF-I axis and catecholamines. There were no differences in peak exercise heart rate, serum lactate, and peak O2 uptake normalized to lean body mass between the groups. Obesity attenuated the GH response to exercise (8.9 +/- 1.1 vs. 3.4 +/- 0.7 ng/ml in NW and Ob participants, respectively; P < 0.02). No significant differences in the response to exercise were found for other components of the GH-IGF-I axis. Obesity attenuated the catecholamine response to exercise (epinephrine: 52.5 +/- 12.7 vs. 18.7 +/- 3.7 pg/ml, P < 0.02; norepinephrine: 479.5 +/- 109.9 vs. 218.0 +/- 26.0 pg/ml, P < 0.04; dopamine: 17.2 +/- 2.9 vs. 3.5 +/- 1.9 pg/ml, P < 0.006 in NW and Ob, respectively). Insulin levels were significantly higher in the obese children and dropped significantly after exercise in both groups. Despite the elevated insulin levels and the blunted counterregulatory response, none of the participants developed hypoglycemia. Childhood obesity was associated with attenuated GH and catecholamine response to acute exercise. These abnormalities were compensated for, so that exercise was not associated with hypoglycemia, despite increased insulin levels in obese children.     

Comparison between voluntary and stimulated contractions of the quadriceps femoris for growth hormone response and muscle damage.

This study aimed to compare voluntary and stimulated exercise for changes in muscle strength, growth hormone (GH), blood lactate, and markers of muscle damage. Nine healthy men had two leg press exercise bouts separated by 2 wk. In the first bout, the quadriceps muscles were stimulated by biphasic rectangular pulses (75 Hz, duration 400 mus, on-off ratio 6.25-20 s) with current amplitude being consistently increased throughout 40 contractions at maximal tolerable level. In the second bout, 40 voluntary isometric contractions were performed at the same leg press force output as the first bout. Maximal voluntary isometric strength was measured before and after the bouts, and serum GH and blood lactate concentrations were measured before, during, and after exercise. Serum creatine kinase (CK) activity and muscle soreness were assessed before, immediately after, and 24, 48, and 72 h after exercise. Maximal voluntary strength decreased significantly (P < 0.05) after both bouts, but the magnitude of the decrease was significantly (P < 0.05) greater for the stimulated contractions (-22%) compared with the voluntary contractions (-9%). Increases in serum GH and lactate concentrations were significantly (P < 0.05) larger after the stimulation compared with the voluntary exercise. Increases in serum CK activity and muscle soreness were also significantly (P < 0.05) greater for the stimulation than voluntary exercise. It was concluded that a single bout of electrical stimulation exercise resulted in greater GH response and muscle damage than voluntary exercise.     

Cytokine response to strenuous exercise in athletes and non-athletes--an adaptive response

Exercise and physical strenuous activity have been demonstrated to increase the serum TNF-alpha and IL-6. Regular physical training is expected to attenuate such a response. This study was undertaken to understand the impact of regular exercise training on IL-6 and TNF-alpha in athletes and non-athletes. Ten athletes, who have been on regular training for the past 6 months, and 10 age- and sex-matched subjects (non-athlete group) who had no practice of regular exercise, were recruited. Both were subjected to undergo the same frequency level of strenuous exercise. Blood samples were collected; one before strenuous exercise and the other after the exercise. Plasma cytokines, IL-6 and TNF-alpha, were estimated using Sandwich ELISA method. All participants in the study were male with the athletes' age being 18.00+/-1.3years (mean+/-SD) and the non-athletes were aged 20.00+/-0.6years (mean+/-SD). Majority of the athletes and non-athletes demonstrated a rise in IL-6 and a fall in TNF-alpha levels. Further, the athletes showed a lesser magnitude of change in the cytokine levels following a longer duration of exercise than non-athletes. Athletes appear to have an attenuated cytokine response. Regular physical training has been demonstrated to attenuate the immune response to exercise in either direction.     

Platelet aggregation, lipids and excretion of catecholamines after acute physical exercise in patients with myocardial infarction

The effect of acute physical exercise and a four-month conditioning program on cardiovascular risk factors was investigated in patients with myocardial infarction. The bicycle exercise testing caused a moderate rise in urinary epinephrine, serum cholesterol and HDL cholesterol levels. The changes in platelet aggregation and urinary catecholamines were markedly greater in the group with exercise induced ischaemic changes. Under the effect of the conditioning program a significant improvement in the performance capacity and circulatory response could be observed. The direction of changes in platelet aggregation and in the lipid parameters were favourable too.     

Vitamin D Status and Hypocalcemic Response to Protamine in Exercised and Non-exercised Dairy Cows

Bone resorption was studied in post parturient cows using intravenous injection of protamine. Protamine inhibits bone resorption and the protamine-induced hypocalcemia can be taken as a measure of this process. The studies were performed in a herd where half of the cows had been tied indoors for 21/2 years, the other half had been given daily exercise during the same period. All animals were fed in the same way. The hypocalcémie response to protamine was the same in both groups, which indicates that exercise did not change bone resorption. The serum levels of calcium, inorganic phosphorus and magnesium around parturition did not differ. The daily exposure to daylight increased the serum level of 25-(OH)-chole-calciferol in late summer in the exercised group.     

Increased lymphocyte antioxidant defences in response to exhaustive exercise do not prevent oxidative damage

It has been reported that exercise induces oxidative stress and causes adaptations in antioxidant defences. The aim of this study was to determine the adaptations of lymphocytes to the oxidative stress induced by an exhaustive exercise. Nine voluntary male subjects participated in the study. The exercise was a cycling mountain stage (171.8 km), and the cyclists took a mean of 283 min to complete it. Blood samples were taken the morning of the cycling stage day, after overnight fasting, and 3 h after finishing the stage. We determined the blood glutathione redox status (GSSG/GSH), lymphocyte antioxidant enzyme activities and superoxide dismutase (SOD) levels; the plasma and lymphocyte vitamin E levels; the serum lactate dehydrogenase (LDH) and creatine kinase (CK) activities and urate levels; the plasma carotene and malonaldehyde (MDA) levels; and the lymphocyte carbonyl index. The cycling stage induced significant increases in blood-oxidized (glutathione/GSSG), plasma MDA and serum urate levels. The exercise also produced increases in CK and LDH serum activities. The mountain cycling stage induced significant increases in lymphocyte vitamin E levels, glutathione peroxidase and glutathione reductase activities as well as increased SOD activity and protein levels. The protein carbonyl levels increased significantly in lymphocytes after the stage. In conclusion, in spite of increasing antioxidant defences in response to the oxidative stress induced by the exhaustive exercise, lymphocyte oxidative damage was produced after the stage as demonstrated by the increased carbonyl index even in very well trained athletes.     

Acute exercise has no effect on ghrelin plasma concentrations.

Exercise is a potent, dose-dependent stimulus of growth hormone (GH) secretion. The hypothalamic peptides, GH-releasing hormone (GHRH) and somatostatin are regarded as major regulators of this stimulation. The role of the stomach-derived peptide ghrelin, which has been shown to exert strong GH releasing effects, has not been fully characterized yet. We therefore studied GH and ghrelin plasma concentrations in response to graded levels of exercise in eight healthy young volunteers. After determination of their individual maximal exercise capacity, all individuals underwent a treadmill exercise at 50 %, 70 %, and 90 % of maximum oxygen consumption (VO (2)max) on different days. Maximal GH response to exercise was observed after 40 minutes at 50 % VO (2)max and after 20 minutes at 70 and 90 % VO (2max). GH serum concentrations increased significantly at all three exercise intensities (GH peak concentrations were 5.8 +/- 2.3 ng/ml, 12.0 +/- 3.2 ng/ml, and 9.8 +/- 4.7 ng/ml, respectively). In contrast, ghrelin plasma concentrations remained unchanged at all three workloads. Assuming that the sensitivity of the GH neuroendocrine/metabolic regulation of GH is unaltered, ghrelin does not participate in the regulation of the GH response to exercise in healthy males.     

Interconnection of carbohydrate and lipid metabolism in various modes of muscle activity

The activity of hexokinase and lipase has been determined in skeletal muscles of different metabolic types and adipose tissue of untrained albino rats during two variations of predominant aerobic physical exercise: long-term swimming and long-term swimming including short-term loads (20 s) of maximal intensity (acceleration). Muscle and liver glycogen depletion, serum lactate, glucose and free fatty acids concentrations are also investigated. It is shown that long-term swimming (first variation) has promoted a decrease of both enzymatic activities in muscle fibres and an increase in lipolytic activity of the adipose tissue. During the physical exercise with the acceleration an increase in hexokinase activity occurs in response to 20 min swimming, with its maximal decrease in response to 40 min of exercise. Activity of lipase in slow-twitch oxidative fibres of soleus and in the adipose tissue increases from 20 min to the end of the exercise. Depletion of glycogen in the muscles and liver is determined in fast-twitch oxidative-glycolytic fibres and in the liver in two types of exercises, being more significant in muscles after exercise with accelerations. Concentrations of serum lactate, glucose and free fatty acids remain unchanged after both variations of swimming. So, it may be concluded that acute adaptation to the predominant aerobic physical exercise with activity under short-term loads of maximal intensity has induced a rise of the capacity of oxidative muscles to utilise endogenous and exogenous carbohydrate and lipid reserves.     

Serum and urinary markers of skeletal muscle tissue damage after weight lifting exercise

The purpose of this study was to determine whether high intensity weight lifting exercise produces elevations of urinary 3-methylhistidine (3-MH), serum creatine kinase activity (CK), and serum myoglobin concentration (MY), and whether trained weight lifters differed in such responses when compared to a group of untrained subjects. Ten experienced male weight lifters (EWL) and seven untrained male subjects (IWL) performed three sets of six weight lifting exercises at 70%-80% of 1 RM. All subjects consumed a meat-free diet. The 3-MH:creatinine (3-MH:CR) values decreased 24 h and 48 h following exercise (P less than 0.05). The 12-h and 24-h postexercise CK response and the 12-h postexercise MY response increased for both EWL and IWL (P less than 0.05). However, EWL had a lower 24-h postexercise CK response and lower 12-h and 24-h postexercise MY responses compared to IWL (P less than 0.05). Within 48 h following weight lifting exercise, skeletal muscle protein degradation (as assessed by 3-MH:CR values) decreased regardless of prior training experience whereas skeletal muscle tissue damage (as assessed by CK and MY responses) increased. However, prior weight lifting training appeared to diminish the extent of muscle tissue damage.     

Acute exercise effect on postabsorptive serum leptin.

We postulated that high circulating cortisol levels during intense exercise would lead to increased serum leptin concentrations. Young, lean men ate a small meal and then exercised on a cycle ergometer for 41 min or rested on a control day. Serum leptin concentration was 10% greater during exercise than in the control condition (P < 0.05). Directly after exercise, serum leptin dropped to approximately 10% less than the control level (P < 0.05) but had recovered to the nonexercised level after approximately 2 h of recovery. Rapid exercise effects on circulating leptin were related to changes in hemoconcentration rather than changes in leptin mass. When serum leptin was normalized to serum protein, leptin increased by 10% in the exercise condition compared with control by the end of recovery (P < 0.05). Although exercise increased serum cortisol concentration threefold, there was no relation between differences in cortisol and exercise vs. control differences in normalized leptin. The increased leptin mass after exercise may have been related to greater plasma glucose concentration during recovery after exercise compared with the control condition.     

Metabolic changes following eccentric exercise in trained and untrained men

The effects of one 45-min bout of high-intensity eccentric exercise (250 W) were studied in four male runners and five untrained men. Plasma creatine kinase (CK) activity in these runners was higher (P less than 0.001) than in the untrained men before exercise and peaked at 207 IU/ml 1 day after exercise, whereas in untrained men the maximum was 2,143 IU/ml 5 days after exercise. Plasma interleukin-1 (IL-1) in the trained men was also higher (P less than 0.001) than in the untrained men before exercise but did not significantly increase after exercise. In the untrained men, IL-1 was significantly elevated 3 h after exercise (P less than 0.001). In the untrained group only, 24-h urines were collected before and after exercise while the men consumed a meat-free diet. Urinary 3-methylhistidine/creatinine in the untrained group rose significantly from 127 mumol/g before exercise to 180 mumol/g 10 days after exercise. The results suggest that in untrained men eccentric exercise leads to a metabolic response indicative of delayed muscle damage. Regularly performed long distance running was associated with chronically elevated plasma IL-1 levels and serum CK activities without acute increases after an eccentric exercise bout.